The nature and location of the neural substrates damage to which produces hyperphagia and obesity will be explored using symmetrical and asymmetrical knife cuts to the brain, fiber-of-passage sparing brain lesions, and central infusions of norepinephrine, each in conjunction with central vagotomy, full and selective coeliac branch vagotomy, and section of the common nerve to the pancreas. Hypothalamic obesity will also be compared with dietary obesity. The effects of starvation and forced feeding upon the traditional glucoprivic and dipsogenic challenges will be explored. The interaction of activity and obesity will be examined. Finally, our new fiber-of-passage sparing MSG brain lesioning techniques will be verified redundantly and explored parametrically.